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  1. Article ; Online: Crosstalk between autophagy and DNA repair systems.

    Demirbağ-Sarikaya, Sinem / Çakir, Hatice / Gözüaçik, Devrim / Akkoç, Yunus

    Turkish journal of biology = Turk biyoloji dergisi

    2021  Volume 45, Issue 3, Page(s) 235–252

    Abstract: Autophagy and DNA repair are two essential biological mechanisms that maintain cellular homeostasis. Impairment of these mechanisms was associated with several pathologies such as premature aging, neurodegenerative diseases, and cancer. Intrinsic or ... ...

    Abstract Autophagy and DNA repair are two essential biological mechanisms that maintain cellular homeostasis. Impairment of these mechanisms was associated with several pathologies such as premature aging, neurodegenerative diseases, and cancer. Intrinsic or extrinsic stress stimuli (e.g., reactive oxygen species or ionizing radiation) cause DNA damage. As a biological stress response, autophagy is activated following insults that threaten DNA integrity. Hence, in collaboration with DNA damage repair and response mechanisms, autophagy contributes to the maintenance of genomic stability and integrity. Yet, connections and interactions between these two systems are not fully understood. In this review article, current status of the associations and crosstalk between autophagy and DNA repair systems is documented and discussed.
    Language English
    Publishing date 2021-06-23
    Publishing country Turkey
    Document type Journal Article
    ZDB-ID 2046470-8
    ISSN 1303-6092 ; 1300-0152
    ISSN (online) 1303-6092
    ISSN 1300-0152
    DOI 10.3906/biy-2103-51
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress.

    Demirbag-Sarikaya, Sinem / Akkoc, Yunus / Turgut, Sıla / Erbil-Bilir, Secil / Kocaturk, Nur Mehpare / Dengjel, Joern / Gozuacik, Devrim

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 8134

    Abstract: The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved ... ...

    Abstract The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved stress response pathway that is activated by various insults including DNA damage. All sorts of damage to DNA potentially cause loss of genetic information and trigger genomic instability. Most of these lesions are repaired by the activation of DNA damage response following DNA repair mechanisms. Here we describe, a novel protein complex containing the autophagy protein ATG5 and the non-homologous end-joining repair system proteins. We discovered for the first time that ATG5 interacted with both Ku80 (XRCC5) and Ku70 (XRCC6). This novel interaction is facilitated mainly via Ku70. Our results suggest that this interaction is dynamic and enhanced upon genotoxic stresses. Strikingly, we identified that ATG5-Ku70 interaction is necessary for DNA repair and effective recovery from genotoxic stress. Therefore, our results are demonstrating a novel, direct, dynamic, and functional interaction between ATG5 and Ku70 proteins that plays a crucial role in DNA repair under genotoxic stress conditions.
    MeSH term(s) Antigens, Nuclear/genetics ; Antigens, Nuclear/metabolism ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; DNA Damage ; DNA End-Joining Repair ; DNA Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Genomic Instability ; Humans ; Ku Autoantigen/metabolism
    Chemical Substances ATG5 protein, human ; Antigens, Nuclear ; Autophagy-Related Protein 5 ; DNA-Binding Proteins ; Ku Autoantigen (EC 4.2.99.-)
    Language English
    Publishing date 2022-05-17
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-11704-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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